Abstract

Lactate levels have been found to be elevated in many critical diseases. Often prognosis is inversely related to lactate elevation. Salbutamol is frequently given for patient in respiratory distress from various etiologies. There have been many previous studies that have seen an elevation in lactate levels after salbutamol was given. Salbutamol creates a hyperadrenergic condition which increases glycogenolysis and gluconeogenesis and increases glucose, glycolysis, and pyruvate. The excess pyruvate is reduced to lactate since lipolysis and the increase in free fatty acids inhibit the pyruvate dehydrogenase enzyme, preventing pyruvate from entering the Krebs cycle. It is unclear whether salbutamol-associated lactic acidosis is due to the pharmacological properties of salbutamol or because the disease process causes lactic acidosis from hypoxia and increased activity of respiratory muscles.

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